Pituitary adenomas can be classified according to staining affinities of the cell cytoplasm, size, endocrine activity, histologic characteristics, hormone production and contents, ultrastructural features, granularity of the cell cytoplasm, cellular composition, cytogenesis, and growth pattern. Recent classifications, however, omit criteria based on tinctorial stains (i.e., acidophilic, basophilic, and chromophobic) because of the poor correlation between staining affinities of the cell cytoplasm and other pathological features of pituitary tumors, such as the type of hormone produced and cellular derivation.[1,2] A unifying pituitary adenoma classification incorporates the histological, immunocytochemical, and electron microscopic studies of the tumor cells, and stresses the importance of hormone production, cellular composition, and cytogenesis. This classification emphasizes the structure-function relationship and attempts to correlate morphologic features with secretory activity.
Pituitary adenomas are also classified according to size as microadenomas or macroadenomas. Microadenomas are less than 10 mm in their largest diameter, whereas macroadenomas are 10 mm or more in their largest diameter. (See Stage Information for more information.) In addition, pituitary adenomas may be distinguished anatomically as intrapituitary, intrasellar, diffuse, and invasive. Invasive adenomas, which account for approximately 35% of all pituitary neoplasms, may invade into the dura mater, cranial bone, or sphenoid sinus.
Incidence and Presentation
Craniopharyngiomas are relatively rare pediatric tumors, accounting for about 6% of all intracranial tumors in children.[1,2,3] They are believed to be congenital in origin, arising from ectodermal remnants, Rathke cleft, or other embryonal epithelium in the sellar and/or parasellar area. No predisposing factors have been identified.
Because craniopharyngiomas occur in the region of the pituitary gland, endocrine function and growth may be affected. Additionally,...
Lactotroph adenomas secrete prolactin (PRL) and are typically an intrasellar tumor. In women, these adenomas are often small (<10 mm). In either sex, however, they can become large enough to enlarge the sella turcica. These adenomas represent the most common hormone-producing pituitary tumors and account for 25% to 41% of tumor specimens.
Corticotroph (ACTH-Producing) Adenomas
The major manifestation of the corticotroph adenoma is secretion of adrenocorticotropic hormone (ACTH), which results in Cushing syndrome. These tumors are initially confined to the sella turcica, but they may enlarge and become invasive after bilateral adrenalectomy (i.e., Nelson syndrome). These adenomas represent the second or third most common hormone-producing pituitary tumors, depending on the series; in one series, these tumors accounted for 10% of all tumor specimens.[1,4]
Somatotroph (GH-Producing) Adenomas
Somatotroph adenomas produce growth hormone (GH), resulting in gigantism in younger patients and acromegaly in others. Suprasellar extension is not uncommon. These adenomas represent the second or third most common hormone-producing pituitary tumors, depending on the series; in one series these adenomas accounted for 13% of tumor specimens.[1,4]
Thyrotroph (TSH-Producing) Adenomas
Thyrotrophadenomas secrete thyroid-stimulating hormone (TSH), also known as thyrotropin, which results in hyperthyroidism without TSH suppression. Many are large and invasive, may be plurihormonal, and secrete both GH and/or PRL. These tumors are rare and account for ?2% of tumor specimens.[1,4,5]
Gonadotroph adenomas may secrete follicle-stimulating hormone (FSH) and/or luteinizing hormone (LH), or the alpha or beta subunits that comprise these heterodimers, which, depending on gender, may result in ovarian overstimulation, increased testosterone levels, testicular enlargement, and pituitary insufficiency caused by compression of the pituitary stalk or destruction of normal pituitary tissue by tumor. Many gonadotroph tumors, however, are unassociated with clinical or biochemical evidence of hormone excess and may be considered to be nonfunctioning or endocrine-inactive tumors. Functional, clinically detectable gonadotroph adenomas are rare.